Decreased urinary active and inactive kallikrein by chronic infusion of vasopressin in conscious rats.

To assess possible interactions of circulating vasopressin with the synthesis or activation of renal kallikrein, we studied the effect of chronic infusion of vasopressin (7.2 U/kg/day i.p.) for 6 days on the urinary excretion of total and active kallikrein in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after the treatment with trypsin (200 micrograms/ml). Chronic infusion of vasopressin induced sustained decreases in urinary total, active and inactive kallikrein excretion, but did not affect the ratio of active to total kallikrein. The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1 +/- 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5 +/- 14.6 pg/ml in vehicle-infused rats (n = 7), p less than 0.001) and in weight gain (39.6 +/- 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 +/- 3.3 g in vehicle-infused rats (n = 7), p less than 0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Circulating levels of angiotensin II was decreased by chronic infusion of vasopressin. Thus, the present study suggests that the elevation of circulating vasopressin levels induces a decrease in the synthesis of renal kallikrein.